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  • Frontiers Media SA  (16)
  • Chen, Hao  (16)
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  • Frontiers Media SA  (16)
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  • 1
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    Data_Sheet_1.docx
    Frontiers Media SA ; 2022
    In:  Frontiers in Cardiovascular Medicine Vol. 9 ( 2022-4-11)
    Details
    In: Frontiers in Cardiovascular Medicine, Frontiers Media SA, Vol. 9 ( 2022-4-11)
    Abstract: Cardiovascular diseases (CVD) are the leading cause of death worldwide, wherein myocardial infarction (MI) is the most dangerous one. Promoting angiogenesis is a prospective strategy to alleviate MI. Our previous study indicated that profilin 2 (PFN2) may be a novel target associated with angiogenesis. Further results showed higher levels of serum PFN2 and exosomal PFN2 in patients, mice, and pigs with MI. In this study, we explored whether PFN2 and endothelial cell (EC)-derived exosomal PFN2 could increase angiogenesis and be beneficial for the treatment of MI. Serum PFN2, exosomes, and exosomal PFN2 were elevated in rats with MI. PFN2 and exosomes from PFN2-overexpressing ECs (OE-exo) enhanced EC proliferation, migration, and tube formation ability. OE-exo also significantly increased the vessel number in zebrafish and protected the ECs from inflammatory injury. Moreover, OE-exo-treated mice with MI showed improvement in motor ability, ejection fraction, left ventricular shortening fraction, and left ventricular mass, as well as increased vessel numbers in the MI location, and decreased infarction volume. Mechanistically, PI3K might be the upstream regulator of PFN2, while ERK might be the downstream regulator in the PI3K-PFN2-ERK axis. Taken together, our findings demonstrate that PFN2 and exosomal PFN2 promote EC proliferation, migration, and tube formation through the PI3K-PFN2-ERK axis. Exosomal PFN2 may be a valuable target in the repair of MI injury via angiogenesis.
    Type of Medium: Online Resource
    ISSN: 2297-055X
    URL: Article
    URL: Article
    DOI: 10.3389/fcvm.2022.781753
    DOI: 10.3389/fcvm.2022.781753.s001
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2781496-8
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  • 2
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    Table_4.xlsx
    Frontiers Media SA ; 2024
    In:  Frontiers in Nutrition Vol. 10 ( 2024-1-8)
    Details
    In: Frontiers in Nutrition, Frontiers Media SA, Vol. 10 ( 2024-1-8)
    Abstract: Chronic kidney disease (CKD) is often accompanied by alterations in the metabolic profile of the body, yet the causative role of these metabolic changes in the onset of CKD remains a subject of ongoing debate. This study investigates the causative links between metabolites and CKD by leveraging the results of genomewide association study (GWAS) from 486 blood metabolites, employing bulk two-sample Mendelian randomization (MR) analyses. Building on the metabolites that exhibit a causal relationship with CKD, we delve deeper using enrichment analysis to identify the metabolic pathways that may contribute to the development and progression of CKD. Methods In conducting the Mendelian randomization analysis, we treated the GWAS data for 486 metabolic traits as exposure variables while using GWAS data for estimated glomerular filtration rate based on serum creatinine (eGFRcrea), microalbuminuria, and the urinary albumin-to-creatinine ratio (UACR) sourced from the CKDGen consortium as the outcome variables. Inverse-variance weighting (IVW) analysis was used to identify metabolites with a causal relationship to outcome. Using Bonferroni correction, metabolites with more robust causal relationships are screened. Additionally, the IVW-positive results were supplemented with the weighted median, MR-Egger, weighted mode, and simple mode. Furthermore, we performed sensitivity analyses using the Cochran Q test, MR-Egger intercept test, MR-PRESSO, and leave-one-out (LOO) test. Pathway enrichment analysis was conducted using two databases, KEGG and SMPDB, for eligible metabolites. Results During the batch Mendelian randomization (MR) analyses, upon completion of the inverse-variance weighted (IVW) approach, sensitivity analysis, and directional consistency checks, 78 metabolites were found to meet the criteria. The following four metabolites satisfy Bonferroni correction: mannose, N-acetylornithine, glycine, and bilirubin (Z, Z), and mannose is causally related to all outcomes of CKD. By pathway enrichment analysis, we identified eight metabolic pathways that contribute to CKD occurrence and progression. Conclusion Based on the present analysis, mannose met Bonferroni correction and had causal associations with CKD, eGFRcrea, microalbuminuria, and UACR. As a potential target for CKD diagnosis and treatment, mannose is believed to play an important role in the occurrence and development of CKD.
    Type of Medium: Online Resource
    ISSN: 2296-861X
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    DOI: 10.3389/fnut.2023.1274078
    DOI: 10.3389/fnut.2023.1274078.s001
    DOI: 10.3389/fnut.2023.1274078.s002
    DOI: 10.3389/fnut.2023.1274078.s003
    DOI: 10.3389/fnut.2023.1274078.s004
    DOI: 10.3389/fnut.2023.1274078.s005
    DOI: 10.3389/fnut.2023.1274078.s006
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2024
    detail.hit.zdb_id: 2776676-7
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  • 3
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    Table_1.xlsx
    Frontiers Media SA ; 2023
    In:  Frontiers in Plant Science Vol. 14 ( 2023-7-17)
    Details
    In: Frontiers in Plant Science, Frontiers Media SA, Vol. 14 ( 2023-7-17)
    Abstract: Solanum torvum (Swartz) (2n = 24) is a wild Solanaceae plant with high economic value that is used as a rootstock in grafting for Solanaceae plants to improve the resistance to a soil-borne disease caused by root-knot nematodes (RKNs). However, the lack of a high-quality reference genome of S . torvum hinders research on the genetic basis for disease resistance and application in horticulture. Herein, we present a chromosome-level assembly of genomic sequences for S . torvum combining PacBio long reads (HiFi reads), Illumina short reads and Hi-C scaffolding technology. The assembled genome size is ~1.25 Gb with a contig N50 and scaffold N50 of 38.65 Mb and 103.02 Mb, respectively as well as a BUSCO estimate of 98%. GO enrichment and KEGG pathway analysis of the unique S . torvum genes, including NLR and ABC transporters, revealed that they were involved in disease resistance processes. RNA-seq data also confirmed that 48 NLR genes were highly expressed in roots and fibrous roots and that three homologous NLR genes ( Sto0288260.1 , Sto0201960.1 and Sto0265490.1 ) in S. torvum were significantly upregulated after RKN infection. Two ABC transporters, ABCB9 and ABCB11 were identified as the hub genes in response to RKN infection. The chromosome-scale reference genome of the S . torvum will provide insights into RKN resistance.
    Type of Medium: Online Resource
    ISSN: 1664-462X
    URL: Article
    URL: Article
    URL: Article
    DOI: 10.3389/fpls.2023.1210513
    DOI: 10.3389/fpls.2023.1210513.s001
    DOI: 10.3389/fpls.2023.1210513.s002
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2023
    detail.hit.zdb_id: 2687947-5
    detail.hit.zdb_id: 2613694-6
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  • 4
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    Image_2.tif
    Frontiers Media SA ; 2022
    In:  Frontiers in Immunology Vol. 12 ( 2022-1-24)
    Details
    In: Frontiers in Immunology, Frontiers Media SA, Vol. 12 ( 2022-1-24)
    Abstract: Chronic allograft dysfunction (CAD) is the major cause of late graft loss in long-term renal transplantation. In our previous study, we found that epithelial–mesenchymal transition (EMT) is a significant event in the progression of renal allograft tubulointerstitial fibrosis, and impaired autophagic flux plays a critical role in renal allograft fibrosis. Everolimus (EVR) has been reported to be widely used to prevent the progression of organ fibrosis and graft rejection. However, the pharmacological mechanism of EVR in kidney transplantation remains to be determined. We used CAD rat model and the human kidney 2 (HK2) cell line treated with tumor necrosis factor-α (TNF-α) and EVR to examine the role of EVR on TNF-α-induced EMT and transplanted renal interstitial fibrosis. Here, we found that EVR could attenuate the progression of EMT and renal allograft interstitial fibrosis, and also activate autophagy in vivo . To explore the mechanism behind it, we detected the relationship among EVR, autophagy level, and TNF-α-induced EMT in HK2 cells. Our results showed that autophagy was upregulated upon mTOR pathway inhibition by EVR, which could significantly reduce expression of TNF-α-induced EMT. However, the inhibition of EVR on TNF-α-induced EMT was partly reversed following the addition of autophagy inhibitor chloroquine. In addition, we found that TNF-α activated EMT through protein kinase B (Akt) as well as nuclear factor kappa B (NF-κB) pathway according to the RNA sequencing, and EVR’s effect on the EMT was only associated with IκB-α stabilization instead of the Akt pathway. Together, our findings suggest that EVR may retard impaired autophagic flux and block NF-κB pathway activation, and thereby prevent progression of TNF-α-induced EMT and renal allograft interstitial fibrosis.
    Type of Medium: Online Resource
    ISSN: 1664-3224
    URL: Article
    URL: Article
    URL: Article
    DOI: 10.3389/fimmu.2021.753412
    DOI: 10.3389/fimmu.2021.753412.s001
    DOI: 10.3389/fimmu.2021.753412.s002
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2606827-8
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  • 5
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    Impaired ATG16L-Dependent Autophagy Promotes Renal Interstitial Fibrosis in Chronic Renal Graft Dysfunction Through Inducing EndMT by NF-κB Signal Pathway
    Frontiers Media SA ; 2021
    In:  Frontiers in Immunology Vol. 12 ( 2021-4-13)
    Details
    In: Frontiers in Immunology, Frontiers Media SA, Vol. 12 ( 2021-4-13)
    Abstract: Chronic renal graft dysfunction (CAD) is caused by multiple factors, including glomerular sclerosis, inflammation, interstitial fibrosis and tubular atrophy (IF/TA). However, the most prominent elements of CAD are IF/TA. Our studies have confirmed that endothelial-mesenchymal transition (EndMT) is an important source to allograft IF/TA. The characteristic of EndMT is the loss of endothelial marker and the acquisition of mesenchymal or fibroblastic phenotypes. Autophagy is an intracellular degradation pathway that is regulated by autophagy-related proteins and plays a vital role in many fibrotic conditions. However, whether or not autophagy contributes to fibrosis of renal allograft and how such mechanism occurs still remains unclear. Autophagy related 16 like gene (ATG16L) is a critical autophagy-related gene (ARG) necessary for autophagosome formation. Here, we first analyzed kidney transplant patient tissues from Gene Expression Omnibus (GEO) datasets and 60 transplant patients from our center. Recipients with stable kidney function were defined as non-CAD group and all patients in CAD group were histopathologically diagnosed with CAD. Results showed that ATG16L, as one significant differential ARG, was less expressed in CAD group compared to the non-CAD group. Furthermore, we found there were less autophagosomes and autolysosomes in transplanted kidneys of CAD patients, and downregulation of autophagy is a poor prognostic factor. In vitro, we found out that the knockdown of ATG16L enhanced the process of EndMT in human renal glomerular endothelial cells (HRGECs). In vivo , the changes of EndMT and autophagic flux were then detected in rat renal transplant models of CAD. We demonstrated the occurrence of EndMT, and indicated that abundance of ATG16L was accompanied by the dynamic autophagic flux change along different stages of kidney transplantation. Mechanistically, knockdown of ATG16L, specifically in endothelial cells, reduced of NF-κB degradation and excreted inflammatory cytokines (IL-1β, IL-6 and TNF-α), which could facilitate EndMT. In conclusion, ATG16L-dependent autophagic flux causing by transplant showed progressive loss increase over time. Inflammatory cytokines from this process promoted EndMT, thereby leading to progression of CAD. ATG16L served as a negative regulator of EndMT and development of renal graft fibrosis, and autophagy can be explored as a potential therapeutic target for chronic renal graft dysfunction.
    Type of Medium: Online Resource
    ISSN: 1664-3224
    URL: Article
    DOI: 10.3389/fimmu.2021.650424
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2021
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  • 6
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    Data_Sheet_1.docx
    Frontiers Media SA ; 2022
    In:  Frontiers in Medicine Vol. 9 ( 2022-5-20)
    Details
    In: Frontiers in Medicine, Frontiers Media SA, Vol. 9 ( 2022-5-20)
    Abstract: Fast and accurate segmentation of knee bone and cartilage on MRI images is becoming increasingly important in the orthopaedic area, as the segmentation is an essential prerequisite step to a patient-specific diagnosis, optimising implant design and preoperative and intraoperative planning. However, manual segmentation is time-intensive and subjected to inter- and intra-observer variations. Hence, in this study, a three-dimensional (3D) deep neural network using adversarial loss was proposed to automatically segment the knee bone in a resampled image volume in order to enlarge the contextual information and incorporate prior shape constraints. A restoration network was proposed to further improve the bone segmentation accuracy by restoring the bone segmentation back to the original resolution. A conventional U-Net-like network was used to segment the cartilage. The ultimate results were the combination of the bone and cartilage outcomes through post-processing. The quality of the proposed method was thoroughly assessed using various measures for the dataset from the Grand Challenge Segmentation of Knee Images 2010 (SKI10), together with a comparison with a baseline network U-Net. A fine-tuned U-Net-like network can achieve state-of-the-art results without any post-processing operations. This method achieved a total score higher than 76 in terms of the SKI10 validation dataset. This method showed to be robust to extract bone and cartilage masks from the MRI dataset, even for the pathological case.
    Type of Medium: Online Resource
    ISSN: 2296-858X
    URL: Article
    URL: Article
    DOI: 10.3389/fmed.2022.792900
    DOI: 10.3389/fmed.2022.792900.s001
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2775999-4
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  • 7
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    Image_2.JPEG
    Frontiers Media SA ; 2023
    In:  Frontiers in Nutrition Vol. 10 ( 2023-3-2)
    Details
    In: Frontiers in Nutrition, Frontiers Media SA, Vol. 10 ( 2023-3-2)
    Abstract: According to the 2021 consensus statement about triglyceride (TG)-rich lipoproteins and their remnants from the European Atherosclerosis Society (EAS), fasting TG level & lt; 1.2 mmol/L is regarded as optimal, otherwise considered as non-optimal TG (NoTG). However, the postprandial cut-off value after a daily meal corresponding to a fasting TG level of 1.2 mmol/L has not been explored. Materials and methods Six hundred and eighteen inpatients aged 18 to 70 were recruited in this study. Among them, 219 subjects had fasting TG levels & lt; 1.2 mmol/L (i.e., OTG group), and 399 subjects had fasting TG levels ≥ 1.2 mmol/L (i.e., NoTG group). Serum levels of blood lipids, including calculated non-high-density lipoprotein cholesterol (non-HDL-C) and remnant cholesterol (RC), were monitored at 0, 2, and 4 h after a daily Chinese breakfast according to their dietary habits. Receiver operating characteristic (ROC) curve analysis was used to determine the postprandial cut-off value corresponding to the fasting TG level of 1.2 mmol/L. Kappa statistics were performed to determine the consistency between fasting and postprandial cut-off values in determining whether TG was optimal. Univariate and multivariate logistic regression analyses were conducted to evaluate the associations between NoTG and potential confounders. Subgroup analyses were performed to explore the association between postprandial TG levels at 4h (pTG4h) and NoTG in greater detail. Results Postprandial levels of TG and RC significantly elevated and peaked at 4h after a daily breakfast in two groups ( P & lt; 0.05). The optimal cut-off value at 4h corresponding to fasting TG of 1.2 mmol/L was 1.56 mmol/L. According to the fasting cut-off value, the percentage of patients with NoTG was 64.6% in the fasting state while increasing obviously to 73.3–78.4% at 2 and 4h, respectively, after a daily Chinese breakfast. According to the postprandial cut-off value, the percentage of patients with NoTG at 4h after a daily Chinese breakfast was 62.6% which was close to 64.6% in the fasting state. The Kappa coefficient was 0.551, indicating a moderate consistency between the fasting and postprandial cut-off values in the diagnosis of NoTG. Moreover, the subjects with NoTG determined by the postprandial TG cut-off value had an obviously higher postprandial level of RC (1.2 vs. 0.8 mmol/L) and percentage of HRC (37.1 vs. 32.1%) than those determined by the fasting TG cut-off value. Multivariate logistic regression analyses demonstrated that except for BMI, pTG4h emerged as an independent predictor of not. Subgroup analyses revealed that the association between pTG4h and NoTG was consistent across subgroups. Conclusion Taken together, we for the first time determined TG 1.56 mmol/L as the postprandial cut-off value corresponding to fasting TG 1.2 mmol/L in Chinese subjects. This could make it more convenient to determine whether TG is optimal or not in the fasting or postprandial state.
    Type of Medium: Online Resource
    ISSN: 2296-861X
    URL: Article
    URL: Article
    URL: Article
    DOI: 10.3389/fnut.2023.1037270
    DOI: 10.3389/fnut.2023.1037270.s001
    DOI: 10.3389/fnut.2023.1037270.s002
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2023
    detail.hit.zdb_id: 2776676-7
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  • 8
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    Table3.DOCX
    Frontiers Media SA ; 2022
    In:  Frontiers in Genetics Vol. 12 ( 2022-2-21)
    Details
    In: Frontiers in Genetics, Frontiers Media SA, Vol. 12 ( 2022-2-21)
    Abstract: Background: The occurrence of proteinuria is one of the evaluation indicators of transplanted kidney damage and becomes an independent risk factor for poor prognosis after kidney transplantation. Our research sought to understand these potential associations and detect the underlying impact of single-nucleotide polymorphisms (SNPs) on proteinuria in kidney transplant recipients. Materials and Methods: There were 200 recipients enrolled in this study, from which blood samples were extracted for SNP mutation–related gene detection. RNA sequencing was performed in kidney tissues after kidney transplantation, and the significantly differentially expressed genes (DEGs) were analyzed between the control group and the proteinuria group. Then, the intersection of genes with SNP mutations and DEGs was conducted to obtain the target genes. Multiple genetic models were used to investigate the relationship between SNPs and proteinuria. In addition, the effect of SNP mutation in the target gene was further validated in human renal podocytes. Results: According to the sequencing results, 26 significant SNP mutated genes and 532 DEGs were found associated with proteinuria after kidney transplantation. The intersection of SNP mutated genes and DEGs showed that the Toll-like receptor 2 (TLR2) gene was significantly increased in the transplanted renal tissues of patients with proteinuria after kidney transplantation, which was consistent with the results of immunohistochemical staining. Further inheritance model results confirmed that mutations at rs3804099 of the TLR2 gene had significant influence on the occurrence of proteinuria after kidney transplantation. In the in vitro validation, we found that, after the mutation of rs3804099 on the TLR2 gene, the protein expressions of podocalyxin and nephrin in podocytes were significantly decreased, while the protein expressions of desmin and apoptosis markers were significantly increased. The results of flow cytometry also showed that the mutation of rs3804099 on the TLR2 gene significantly increased the apoptotic rate of podocytes. Conclusion: Our study suggested that the mutation of rs3804099 on the TLR2 gene was significantly related to the generation of proteinuria after kidney transplantation. Our data provide insights into the prediction of proteinuria and may imply potential individualized therapy for patients after kidney transplantation.
    Type of Medium: Online Resource
    ISSN: 1664-8021
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    DOI: 10.3389/fgene.2021.798001
    DOI: 10.3389/fgene.2021.798001.s001
    DOI: 10.3389/fgene.2021.798001.s002
    DOI: 10.3389/fgene.2021.798001.s003
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2606823-0
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  • 9
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    DataSheet_1.pdf
    Frontiers Media SA ; 2021
    In:  Frontiers in Immunology Vol. 12 ( 2021-2-24)
    Details
    In: Frontiers in Immunology, Frontiers Media SA, Vol. 12 ( 2021-2-24)
    Abstract: Costimulatory blockade provides new therapeutic opportunities for ensuring the long-term survival of kidney grafts. The adoption of the novel immunosuppressant Belatacept has been limited, partly due to concerns regarding higher rates and grades of acute rejection in clinical trials. In this study, we hypothesized that a combined therapy, Belatacept combined with BTLA overexpression, may effectively attenuate acute rejection after kidney transplantation. Materials and Methods The rat kidney transplantation model was used to investigate graft rejection in single and combined therapy. Graft function was analyzed by detecting serum creatinine. Pathological staining was used to observe histological changes in grafts. The expression of T cells was observed by immunohistochemistry and flow cytometry. In vitro , we constructed an antigen-stimulated immune response by mixed lymphocyte culture, treated with or without Belatacept and BTLA-overexpression adenovirus, to observe the proliferation of receptor cells and the expression of cytokines. In addition, western blot and qRT-PCR analyses were performed to evaluate the expression of CTLA-4 and BTLA at various time points during the immune response. Results In rat models, combined therapy reduced the serum creatinine levels and prolonged graft survival compared to single therapy and control groups. Mixed acute rejection was shown in the allogeneic group and inhibited by combination treatment. Belatacept reduced the production of DSA and the deposition of C4d in grafts. Belatacept combined with BTLA overexpression downregulated the secretion of IL-2 and IFN-γ, as well as increasing IL-4 and IL-10 expression. We also found that Belatacept combined with BTLA overexpression inhibited the proliferation of spleen lymphocytes. The duration of the elevated expression levels of CTLA-4 and BTLA differentially affected the immune response. Conclusion Belatacept combined with BTLA overexpression attenuated acute rejection after kidney transplantation and prolonged kidney graft survival, which suggests a new approach for the optimization of early immunosuppression after kidney transplantation.
    Type of Medium: Online Resource
    ISSN: 1664-3224
    URL: Article
    URL: Article
    DOI: 10.3389/fimmu.2021.618737
    DOI: 10.3389/fimmu.2021.618737.s001
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2021
    detail.hit.zdb_id: 2606827-8
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  • 10
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    Unsupervised Cerebrovascular Segmentation of TOF-MRA Images Based on Deep Neural Network and Hidden Markov Random Field Model
    Frontiers Media SA ; 2020
    In:  Frontiers in Neuroinformatics Vol. 13 ( 2020-1-10)
    Details
    In: Frontiers in Neuroinformatics, Frontiers Media SA, Vol. 13 ( 2020-1-10)
    Type of Medium: Online Resource
    ISSN: 1662-5196
    URL: Article
    DOI: 10.3389/fninf.2019.00077
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2020
    detail.hit.zdb_id: 2452979-5
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